Scurvy (vitamin C deficiency)

[6] [7]

Definition and overview

Scurvy is the multisystem disease caused by severe deficiency of vitamin C (ascorbic acid), an essential water-soluble vitamin that humans cannot synthesise endogenously. The biochemical pivot is collagen: vitamin C is a cofactor for the enzyme reactions of collagen synthesis, and the collagen defect causes blood-vessel fragility, poor wound healing, mucocutaneous bleedings, hair abnormalities, bone pains, and joint contractures due to periosteal and intra-articular bleeding. [6]

The disease is ancient — it crippled the long sea voyages of the Age of Sail and was the leading cause of death in sailors until James Lind's 1747 trial proved citrus could prevent it — yet it is emphatically not extinct.[3] Modern scurvy is concentrated in at-risk subgroups: isolated elderly people subsisting on a "tea-and-toast" diet, patients with alcohol use disorder, people with anorexia nervosa or autism-spectrum selective eating, those with malabsorption, dialysis-dependent patients, refugees and food-insecure populations, and post-bariatric patients. A 2024 national United States inpatient analysis documented a more than three-fold rise in paediatric scurvy between 2016 and 2020.[2]

[6]

Classification

There is no formal WHO or consensus severity grading for scurvy, but examiners expect you to classify it along three axes: [1]

Epidemiology and risk factors

Scurvy develops after more than 1 to 3 months of severe dietary vitamin C deficiency. Because vitamin C is concentrated in fresh fruit and vegetables — the roughly 60 mg daily requirement can be met by a single medium-sized orange — scurvy is a disease of inadequate fresh fruit and vegetable intake, typically in monotonous diets, in advanced age, homelessness and food insecurity, rather than of total starvation per se. [6][9]

[6] [2] [8]

The 2024 JAAOS Global national analysis of 19,413,465 paediatric inpatient records showed the incidence rose from 8.2 to 26.7 per 100,000 over five years, with affected children more likely to be young, male, obese, in the lowest income quartile, and to carry a concurrent diagnosis of autism spectrum disorder — 64.2% in this cohort.[2] Adults follow a different epidemiology: classical stems in exams centre on the isolated elderly patient with a tea-and-toast diet, the chronic alcoholic, the young woman with restrictive anorexia nervosa, and the long-term haemodialysis patient.[5]

Pathophysiology

The mechanism is one of the most examinable in nutrition dermatology because it ties biochemistry directly to a visible phenotype. L-ascorbic acid is a cofactor for the enzyme reactions of collagen synthesis: hydroxylation of proline residues stabilises the collagen triple helix at body temperature, while hydroxylation of lysine permits the inter- and intra-molecular cross-linking that gives tensile strength to mature collagen fibrils. When vitamin C is absent, hydroxylation fails: collagen undergoes structural alterations, osteoid matrix formation is defective and bone resorption increases — producing fragile capillary walls, defective bone and dentin, and twisted, fragmented hair shafts. [6][9]

• Capillary fragility — weakened endothelial basement membrane and perivascular collagen leads to perifollicular petechiae, ecchymoses, and bleeding gums; coagulation factors and platelets are normal, so the bleeding is mechanical, not haematological.
• Poor wound healing — type I and type III collagen cannot be remodelled; chronic ulcers granulate poorly, and previously healed wounds may reopen.
• Defective dentin and bone — in children, osteoid and dentin formation fail, producing sub-periosteal haemorrhage, the radiographic white line, and loose teeth.
• Corkscrew hairs — defective cross-linking in cortical keratin causes the hair shaft to twist, coil, and fragment within a keratin-plugged follicle; this is the pathognomonic cutaneous sign.
• Non-collagen roles — ascorbate is also a cofactor for dopamine β-hydroxylase (catecholamine synthesis — explaining the early fatigue and lassitude), for carnitine synthesis (contributing to myalgia and weakness), and it enhances dietary iron absorption (reducing ferric to ferrous iron) and preserves folate in its active form — both relevant to the anaemia of scurvy. [1]

[1]

Kinetics of deficiency and why symptoms take months to appear

The clinical latency of scurvy is fixed by the small size of the body ascorbate pool and its daily turnover. Reference-value modelling assumes metabolic losses of about 50 mg per day in healthy non-smoking men, with recommended intakes set to hold fasting plasma ascorbate near 50 micromol/L. Smokers both turn over about 40% more vitamin C and run mean plasma concentrations about one-third lower than non-smokers, which is why reference bodies set higher intakes for them. The net result: scurvy develops only after more than 1 to 3 months of severe deficiency, and the working NHANES definition of deficiency is a serum concentration under 11.4 micromol/L. This kinetics explains why scurvy is the disease of months of a monotone diet rather than of brief dietary disturbance, why historically it broke out on long sea voyages only after the ship's citrus ran out, and why modern scurvy clusters in patients whose diet has been rigidly narrow for many months — the autistic selective eater, the tea-and-toast widower, and the anorexic young woman. It also explains the speed of recovery: once ascorbate is supplied, properly hydroxylated collagen is again synthesised and symptoms resolve within days. [11][6][8]

Why the bleeding is non-coagulopathic

A favourite viva question is why does the scurvy patient bleed despite normal clotting? The answer is structural, not biochemical. In scurvy the platelet count, fibrinogen, prothrombin time and activated partial thromboplastin time are all normal — reported directly in a published adult case. What fails is the vascular wall: capillary basement membrane and the perivascular collagen sheath depend on ascorbate for collagen maturation. Without it, the vessel wall is mechanically weak, so trivial shearing forces — gravity in the legs, the brush of a toothbrush, the pull of a hair follicle — allow red cells to extravasate. This is also why scurvy will bleed through anticoagulation rather than because of it — a warfarinised patient with scurvy bleeds from both mechanisms simultaneously. [6]

Clinical presentation

Scurvy is one of the great clinical mimics: it can present as a bleeding disorder, an inflammatory arthritis, a limp in a child, or a non-healing ulcer. Examiners deliberately test atypical presentations, so learn the full phenotype, not just the textbook tetrad. [1]

Cutaneous features (the hallmark)

The cutaneous picture is follicular hyperkeratosis, corkscrew hairs, perifollicular purpura, and ecchymoses. Follicular hyperkeratosis produces a rough, sandpaper skin texture over the upper arms, thighs, and buttocks; each hyperkeratotic follicle contains a twisted, coiled, fragmented corkscrew hair — with perifollicular bleeding, one of the pathognomonic signs. Around each affected follicle, a ring of petechial haemorrhage appears (perifollicular purpura), most densely on dependent areas because gravity drives red-cell extravasation through fragile capillary walls. With more advanced disease, larger ecchymoses appear on the limbs from minor trauma, and existing wounds fail to heal or reopen.[6][1]

Oral features

The gums become purple, swollen, spongy, and bleed on the slightest touch. Gingival hypertrophy is most pronounced between the teeth, and in advanced disease the periodontal ligament fails and teeth become loose. Mucosal petechiae may appear on the palate and buccal mucosa. A critical examiner point: gum changes require teeth — the edentulous patient does not develop the classic gingival picture, which can delay diagnosis in elderly edentulous patients.[3]

Systemic features

Musculoskeletal manifestations dominate in children and are often the presenting complaint: arthralgia, myalgia, haemarthrosis and muscular haematomas — present in 80% of cases in one adult series — plus lower-limb pain and refusal to walk. In infants and young children, sub-periosteal haemorrhage produces severe lower limb pain and tenderness — Moeller-Barlow disease. Systemic symptoms include fatigue, malaise, oedema and anaemia; laboratory abnormalities are nonspecific (anaemia, low cholesterol and albumin). [9]

Natural history and order of appearance

Scurvy evolves in a predictable sequence that examiners reward knowing. Early, non-specific symptoms — fatigue, malaise, anorexia, irritability, and low mood — appear first, reflecting impaired catecholamine synthesis (dopamine β-hydroxylase requires ascorbate) and early carnitine deficiency. These are easily attributed to the underlying illness (alcoholism, anorexia, isolation) and are missed. Over the following weeks, follicular hyperkeratosis appears on the extensor limbs, followed by corkscrew hairs within those plugged follicles, and then perifollicular purpura as capillary fragility declares itself. Gingival swelling and bleeding typically follow, and finally the more dramatic manifestations — ecchymoses, haemarthrosis, refusal to walk (children), reopening of old wounds, and anaemia — appear in advanced disease. The lesson for the clinician is that scurvy is symptomatic for weeks before it is haemorrhagic: the alert examiner will pick the corkscrew hair and the perifollicular purpura at the bedside long before the patient develops the bruising that triggers a coagulopathy workup. [1][6]

Comorbidities and co-deficiencies

Scurvy almost never occurs in isolation. The same dietary pattern that produces vitamin C deficiency usually produces thiamine deficiency (Wernicke risk), folate and B12 deficiency (megaloblastic anaemia), iron deficiency (microcytic anaemia), zinc deficiency (acrodermatitis enteropathica pattern), vitamin D deficiency, and protein-energy malnutrition. Alcohol use disorder, anorexia nervosa, malabsorption, and dialysis each carry their own cluster of co-deficiencies. A practical rule is: when you find scurvy, screen for the others — send thiamine (and give empirically before refeeding), folate, B12, iron studies, zinc, vitamin D, and a basic nutritional panel, and arrange dietetic and (where relevant) psychiatric or addiction input. Treating ascorbate alone corrects the collagen defect but leaves the patient exposed to Wernicke, refeeding syndrome, macrocytic anaemia, and osteomalacia. [1][12]

Atypical presentations examiners test

Differential diagnosis

The differential is wide because purpura, limp, and poor wound healing each generate their own lists. The discriminator is the distribution (perifollicular, dependent lower limbs), the corkscrew hair, the dietary history, and a normal coagulation and platelet screen. [1][6]

Clinical and bedside assessment

The diagnosis is essentially clinical and is made at the bedside by combining the dietary history with the characteristic morphology. A focused examination covers skin, gums, joints, and a screen for underlying cause. [1]

The platelet count, prothrombin time and APTT are normal — this combination is the single most useful bedside discriminator from a coagulopathy. [6]

Investigations

Scurvy is a clinical diagnosis confirmed by therapeutic response. Laboratory confirmation is supportive and is not always necessary, but a small panel excludes mimics and quantifies co-deficiencies.[3][6]

[8] [9] [6] [7] [15] [19] [10]

Diagnostic approach and interpretation

In practice the diagnostic sequence is: suspect on clinical grounds (diet + phenotype), exclude mimics with a small panel, confirm by response, and screen for co-deficiencies. Serum vitamin C is the formal diagnostic gold standard, with deficiency defined as a concentration under 11.4 micromol/L — but the assay tends to reflect recent dietary intake, is not always available, and treatment should not be delayed for it. The therapeutic response is the pragmatic standard: published series report symptom resolution within 48 to 96 hours of oral vitamin C at 1 g/day in children and rapid improvement on 500 mg daily in adults, and improvement after starting ascorbate is itself accepted as diagnostic confirmation. The platelet count and coagulation screen are the most important exclusionary tests — a low platelet count, prolonged PT, or prolonged APTT redirects the differential away from scurvy and towards thrombocytopenia, vitamin K deficiency, warfarin excess, liver disease, or disseminated intravascular coagulation. In the limping child, limb radiographs showing the metaphyseal white line, rarefaction zone and sub-periosteal haemorrhage are the radiographic discriminator from septic arthritis, osteomyelitis, and malignancy, and the dietary history is the historical one.[4][6][7][8][10]

Skin biopsy is reserved for the diagnostically uncertain case — typically when the differential includes leukocytoclastic vasculitis or a pigmented purpuric dermatosis. The histological picture is purpura with hyperkeratosis, parakeratosis and follicular plugging — with corkscrew, fragmented hair shafts on biopsy in reported cases — and crucially, no leucocytoclasia and no vessel-wall fibrinoid necrosis — this single distinction separates scurvy from small-vessel vasculitis, which otherwise presents with a similar dependent purpuric phenotype. [15][19]

Management — resuscitation

Scurvy is rarely a time-critical emergency, but several scenarios demand prompt action: severe bleeding or symptomatic anaemia, paediatric refusal to bear weight (which can be the presenting emergency), haemodynamic compromise, and any patient in whom the diagnosis has been missed for months. The immediate bundle is: [1]

[6] [7] [12] [12]

Management — definitive and stepwise

Definitive therapy is ascorbic acid replacement, dietary correction, and treatment of co-deficiencies and the underlying cause. The regimen is straightforward and the response dramatic. [1]

[6] [7] [14] [15] [18] [13]

Dietary correction is the long-term answer and the preventive message. The daily requirement is roughly 60 mg — the amount found in a single medium-sized orange — while the amount necessary to prevent scurvy is only about 7 mg/day (infant reference intakes of 20 mg/day already sit threefold above it). Other fresh produce rich in vitamin C, such as peppers, kiwifruit, strawberries and broccoli, covers the requirement with equal ease; a daily portion of any of these is protective. [6][11]

[7] [6] [17]

Prevention

Scurvy is one of the most easily prevented diseases in medicine — a single daily portion of fruit or vegetables is sufficient. The preventive framework has three layers: adequate dietary intake matched to the regional recommended daily allowance, targeted supplementation in groups with increased requirement or impaired absorption, and anticipatory nutritional counselling of high-risk patients (autistic children with selective eating, the socially isolated elderly, patients on long-term dialysis, and those after bariatric surgery).[3] A focused dietary history at routine encounters — particularly in general practice, paediatric developmental reviews, and pre-dialysis clinics — is the highest-yield preventive intervention, because clinical scurvy is the end-stage of months of a deficient diet during which the patient is asymptomatic but repletable.

The amount necessary to prevent scurvy is only about 7 mg of vitamin C per day — infant reference values (20 mg/day) already sit threefold above it — so almost any diet containing fresh produce is protective. Recommended intakes are set higher to maintain plasma saturation: 75 mg/day for women and 90 mg/day for men in the United States, and 95 to 110 mg/day in the D-A-CH (German, Austrian, Swiss) reference values, which assume metabolic losses of about 50 mg/day and target a fasting plasma ascorbate of 50 micromol/L. Smokers need more — the D-A-CH bodies set 135 mg/day for female and 155 mg/day for male smokers because metabolic turnover is about 40% higher, and NHANES found smokers' mean concentrations about one-third lower than non-smokers. Pregnancy raises the D-A-CH recommendation to 105 mg/day and lactation to 125 mg/day. Dialysis patients warrant routine water-soluble vitamin replacement, but long-term high-dose ascorbate drives oxalate accumulation (see Dialysis-associated scurvy below). Public-health measures that improve access to fresh fruit and vegetables — food subsidies, school fruit schemes, and fortified infant formulas — have historically eliminated scurvy at population scale and remain the structural answer in food-insecure settings. [11][16][8]

Specific subtypes and scenarios

Paediatric scurvy (Moeller-Barlow disease)

Paediatric scurvy is the rising phenotype in modern series and the one most often missed. The 2024 JAAOS Global analysis of 19,413,465 US paediatric inpatients found that incidence rose from 8.2 to 26.7 per 100,000 between 2016 and 2020, and that 64.2% had a concurrent autism spectrum disorder diagnosis.[2] A 2026 series of 21 children (median age 4.4 years, 86% male, all with food selectivity, 80% with autism spectrum disorder) reported a mean 38 days of symptoms before diagnosis, lower limb pain and difficulty walking as the leading features, petechiae and gingivitis, positive acute-phase reactants in half, and compatible radiological findings in 80% — with symptom resolution within 48 to 96 hours of oral vitamin C 1 g/day.[7] Children therefore present with limp, refusal to walk or irritability rather than the textbook cutaneous tetrad, prompting workup for septic arthritis, osteomyelitis, leukaemia or JIA; the radiographic picture — subperiosteal haematoma, ring epiphysis, metaphyseal white line and rarefaction zone, with epiphyseal slips — is the discriminator, and bilateral limb radiographs aid recognition.[10] Vitamin-C-responsive pulmonary hypertension is a rare, potentially lethal paediatric complication.[1]

Scurvy and anorexia nervosa

Scurvy is increasingly recognised in restrictive eating disorders. The 2024 Frontiers in Nutrition review of nine co-occurrence cases highlighted that gastrointestinal, psychiatric, and dermatological symptoms overlap and that diagnosis is often delayed; vitamin C supplementation produces rapid improvement, but the malnutrition of anorexia requires a comprehensive, multidisciplinary, refeeding-safe approach.[5] Always give thiamine before refeeding and monitor phosphate, magnesium, and potassium. [12]

Dialysis-associated scurvy

Vitamin C is water-soluble and is lost during dialysis. A paediatric transplant candidate on haemodialysis developed scurvy with serum ascorbate under 10 micromol/L despite routine supplementation in dialysate and orally, resolving completely on 1 g/day oral.[15] A peritoneal-dialysis adult with a fruit- and vegetable-free diet who had stopped his dialysis vitamin developed a follicular rash confirmed as scurvy on biopsy, resolving completely after ascorbic acid 500 mg twice daily for two weeks.[19] Long-term IV replacement works — 250 mg/week increasing to 500 mg/week corrected deficiency in dialysis patients — but at 500 mg/week the calcium-oxalate saturation threshold was exceeded in 40% of treated patients, so oxalate should be monitored during prolonged supplementation. [13]

Post-bariatric, malabsorptive, and food-insecure scurvy

Gastric bypass and short-bowel syndromes impair absorption of water-soluble as well as fat-soluble vitamins. Refugees, food-insecure households, and socially isolated elderly patients present with the classical phenotype and respond rapidly to oral replacement; the long-term fix is dietary and social. [1]

Complications and pitfalls

The complications of scurvy are the consequences of untreated collagen failure: severe haemorrhage, poor wound healing, reopening of old surgical or traumatic wounds, anaemia, and — in advanced paediatric disease — pulmonary hypertension and death.[1][4]

The classic pitfalls are diagnostic: [1]

Prognosis and disposition

Treated scurvy has an excellent prognosis: symptoms resolve within 48 to 96 hours on oral replacement in children, adult skin lesions clear within about two weeks, and full recovery over weeks is the rule. Untreated scurvy is historically lethal — with no intake the disease can prove fatal within about 5 to 6 months — and modern deaths are rare but described in neglected cases, including children with pulmonary hypertension.[6][7][16][1]

Disposition is usually outpatient with dietetics, social support, and follow-up of co-deficiencies — though 80% of children in a modern series required hospitalisation. Admit patients with severe anaemia, haemodynamic instability, refusal to bear weight (paediatric), suspected pulmonary hypertension, unsafe social circumstances, or significant comorbidity (advanced anorexia, decompensated liver disease). [1][7]

Special populations

[7] [2] [11] [8] [15] [19] [13] [18] [5]

Evidence, guidelines and regional differences

The evidence base is dominated by case series, narrative reviews, and one national inpatient analysis rather than randomised trials — appropriate, since the diagnosis and the cure have been settled for 250 years. The landmark modern papers are: [1]

[6] [14] [16] [8] [6] [3] [4] [10] [11]

Controversies

• Optimal replacement dose — published regimens range from 500 mg to 1 g daily orally in adults and 1 g/day in children, with symptom resolution within 48 to 96 hours; the minimum effective dose has not been formally established. [6][7][14]
• Oral vs IV — oral replacement is standard; a 1.5 g IV loading dose followed by 500 mg orally six-hourly restored levels within 48 hours in critically ill patients with alcohol use disorders. [18]
• Oxalate risk in dialysis — long-term IV ascorbate (500 mg/week) caused calcium-oxalate supersaturation in 40% of dialysis patients; the general tolerable upper intake level is 2 g/day. [13][16]

Exam pearls

[6] [2] [8] [9] [7] [12] [13]

Red flags

Exam application bank (NEET-PG / INICET)

One-line answer

Scurvy is caused by deficiency of vitamin C (ascorbic acid), an essential cofactor for collagen synthesis. Clinical features: follicular hyperkeratosis, corkscrew hairs, perifollicular purpura (capillary fragility from defective collagen), bleeding and hypertrophied gums, poor wound healing, arthralgia, and anaemia. It develops after more than 1 to 3 months of severe deficiency. Risk factors: tea-and-toast diet in the elderly, alcoholism, anorexia nervosa, autism with selective eating, malabsorption, dialysis, smoking, and food insecurity. Treatment: oral ascorbic acid 500 mg to 1 g daily (1 g/day in children) — symptoms resolve typically within days (48 to 96 hours in children); about 7 mg daily prevents scurvy. [6][7][11]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. [1]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. [1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. [1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. [1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. [1]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Scurvy (vitamin C deficiency).

[6] [7] [12] [1]

Quick self-test: a 70-year-old man with corkscrew hairs, perifollicular purpura on the shins, bleeding gums, and a history of living on tea and toast since his wife died. PT 12 s, APTT 31 s, platelets 220. What is the diagnosis, the confirmatory test, and the treatment?

Diagnosis: scurvy (vitamin C deficiency). Confirmatory: serum vitamin C under 11.4 micromol/L, OR the rapid clinical response to vitamin C. Treatment: oral ascorbic acid 500 mg to 1 g daily, plus dietetic referral and social support. Platelets, PT and APTT are normal — bleeding is from capillary fragility, not coagulopathy.

[8] [6] [7] [1] [1]

References

1. [1]Toscano F, Zirilli G, Foti Randazzese S, et al. Scurvy, all the faces you can see: our experience and review of the literature Ital J Pediatr, 2025.PMID 40437614
2. [2]Reikersdorfer KN, Singh A, Young JD, et al. The Troubling Rise of Scurvy: A Review and National Analysis of Incidence, Associated Risk Factors, and Clinical Manifestations J Am Acad Orthop Surg Glob Res Rev, 2024.PMID 39018570
3. [3]Kinlin LM, Weinstein M. Scurvy: old disease, new lessons Paediatr Int Child Health, 2023.PMID 37795755
4. [4]Trapani S, Rubino C, Indolfi G, Lionetti P. A Narrative Review on Pediatric Scurvy: The Last Twenty Years Nutrients, 2022.PMID 35277043
5. [5]Cui S. A comprehensive review on the co-occurrence of scurvy and anorexia nervosa Front Nutr, 2024.PMID 39296506
6. [6]Krečak I, Babić G, Skelin M. Scurvy Acta Dermatovenerol Croat, 2022.PMID 36153722
7. [7]Ramirez IA, Moreno N, Chiaramonte S, Saure C. Scurvy in children with selectivity in foods: experience in a pediatric hospital Medicina (B Aires), 2026.PMID 42604498
8. [8]Schleicher RL, Carroll MD, Ford ES, Lacher DA. Serum vitamin C and the prevalence of vitamin C deficiency in the United States: 2003-2004 National Health and Nutrition Examination Survey (NHANES) Am J Clin Nutr, 2009.PMID 19675106
9. [9]Fain O. Musculoskeletal manifestations of scurvy Joint Bone Spine, 2005.PMID 15797491
10. [10]Agarwal A, Shaharyar A, Kumar A, Bhat MS, Mishra M. Scurvy in pediatric age group - A disease often forgotten? J Clin Orthop Trauma, 2015.PMID 25983516
11. [11]German Nutrition Society (DGE). New Reference Values for Vitamin C Intake Ann Nutr Metab, 2015.PMID 26227083
12. [12]Stanga Z, Brunner A, Leuenberger M, et al. Nutrition in clinical practice-the refeeding syndrome: illustrative cases and guidelines for prevention and treatment Eur J Clin Nutr, 2008.PMID 17700652
13. [13]Canavese C, Petrarulo M, Massarenti P, et al. Long-term, low-dose, intravenous vitamin C leads to plasma calcium oxalate supersaturation in hemodialysis patients Am J Kidney Dis, 2005.PMID 15754276
14. [14]Li R, Byers K, Walvekar RR. Gingival hypertrophy: a solitary manifestation of scurvy Am J Otolaryngol, 2008.PMID 19144306
15. [15]Samonte VA, Sherman PM, Taylor GP, et al. Scurvy diagnosed in a pediatric liver transplant patient awaiting combined kidney and liver retransplantation Pediatr Transplant, 2008.PMID 18331545
16. [16]Bsoul SA, Terezhalmy GT. Vitamin C in health and disease J Contemp Dent Pract, 2004.PMID 15150630
17. [17]Kyprios A. Vitamin C Deficiency Presenting as an Acute Limp in Childhood Cureus, 2020.PMID 32802617
18. [18]Marik PE, Liggett A. Adding an orange to the banana bag: vitamin C deficiency is common in alcohol use disorders Crit Care, 2019.PMID 31077227
19. [19]El Khoury R, Warren M, Ali S, Pirkle JL Jr. An Unexpected Case of Scurvy in a Peritoneal Dialysis Patient Case Rep Nephrol Dial, 2017.PMID 29594144